Why calcium channel blockers could be an elite choice in the treatment of Alzheimer’s disease: a comprehensive review of evidences

Ponne, Saravanaraman; Chinnadurai, Raj Kumar; Boopathy, Rathanam

doi:10.1515/revneuro-2013-0056

Cited by 20 publications

(15 citation statements)

References 154 publications

(146 reference statements)

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“…Hence, CCB's have a good scope in the treatment of cognitive dysfunction and dementia in AD. [14] Flunarizine (FLN) FLN is a highly lipophilic, Class IV, selective, and CCB which also has the ability to block sodium channels, has shown its use in the treatment of a number of neurological and cerebrovascular disorders. [15,16] It is a diphenylmethylpiperazine derivative and is associated with antihistamine hydroxyzine.…”

Section: Role Of Calcium Channel Blockers (Ccb's) In the Treatment Of Admentioning

confidence: 99%

Untitled

Kamili¹

2019

IJGP

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Background: Alzheimer's disease is a chronic, neurodegenerative disease which involves complications in cognitive functioning leading to dementia. Flunarizine (FLN) is a selective, calcium channel blocker that is widely used in the treatment of migraine. Moreover, it was investigated that it can improve cognitive functioning by regulating calcium homeostasis. Objective: The present study aims to evaluate the memory-enhancing effect of FLN in scopolamine-induced dementia model. Materials and Methods: The present study was carried out on male Swiss-albino mice, where Alzheimer's type of dementia was induced by the administration of scopolamine. In the current investigation, the mice were divided into six groups and then test animals received FLN at the doses of 20 mg, 40 mg, and 80 mg after dosing with scopolamine at the dose of 3 mg/kg, intraperitoneally for 7 days. Active avoidance was assessed by the use of elevated plus maze, T-maze, and Morris Water Maze test. The biochemical markers assessed were acetylcholinesterase, catalase, and lipoxygenase activity. Results: FLN at the doses of 20 mg, 40 mg, and 80 mg showed significantly increased impedance in learning and memory with all the tests. Conclusion: The current study demonstrates significant memory-enhancing effect of FLN.

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Section: Role Of Calcium Channel Blockers (Ccb's) In the Treatment Of Admentioning

confidence: 99%

Untitled

Kamili¹

2019

IJGP

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“…CX3CL1 reduces the glutamate mediated excitotoxicity by reducing the influx of Ca 2+ [ 105 ]. Calcium channel blockers also exhibit cognitive enhancing abilities and reduce the risk of dementia genuinely [ 110 ]. Moreover, the application of ion channel blockers with specific antagonists of the NR2B subunit could reduce neurotoxicity significantly [ 111 ].…”

Section: Cx3cl1/cx3cr1 Reduces Excitotoxicitymentioning

confidence: 99%

CX3CL1/CX3CR1 in Alzheimer’s Disease: A Target for Neuroprotection

Chen

Zhao

Guo

et al. 2016

BioMed Research International

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CX3C chemokine ligand 1 (CX3CL1) is an intriguing chemokine belonging to the CX3C family. CX3CL1 is secreted by neurons and plays an important role in modulating glial activation in the central nervous system after binding to its sole receptor CX3CR1 which mainly is expressed on microglia. Emerging data highlights the beneficial potential of CX3CL1-CX3CR1 in the pathogenesis of Alzheimer's disease (AD), a common progressive neurodegenerative disease, and in the progression of which neuroinflammation plays a vital role. Even so, the importance of CX3CL1/CX3CR1 in AD is still controversial and needs further clarification. In this review, we make an attempt to present a concise map of CX3CL1-CX3CR1 associated with AD to find biomarkers for early diagnosis or therapeutic interventions.

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“…Dysregulation of Ca 2+ homeostasis plays a crucial role in the pathogenesis of AD [38][39][40][41][42]. The topic "Calcium channel blockers and dementia" was discussed [43].…”

Section: Drugs Interacting With Ion Channels (Non-receptors)mentioning

confidence: 99%

“…Lu AF20513 (Lundbeck, Valby, DK in collaboration with Otsuka, Tokyo) is a novel AD epitope vaccine, in which the T-helper (Th) cell epitopes of A␤ 42 were replaced by two foreign Th epitopes from tetanus toxoid (TT), P2 and P30, and the immunodominant B-cell epitope of A␤ . Lu AF20513 induced robust non-self T-cell responses and the production of anti-A␤ antibodies that reduced AD-like pathology in the brains of Tg2576 mice without inducing microglial activation [620] (Thomson Reuters Pharma, update of May 15, 2014).…”

Section: Bs-1 Bace Inhibitor Mab Vaccine (Nasvax Ness-ziona Israel mentioning

confidence: 99%

Cognitive Enhancers (Nootropics). Part 3: Drugs Interacting with Targets other than Receptors or Enzymes. Disease-Modifying Drugs. Update 2014

Froestl

Pfeifer

Muhs

2014

JAD

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Scientists working in the field of Alzheimer's disease and, in particular, cognitive enhancers, are very productive. The review "Drugs interacting with Targets other than Receptors or Enzymes. Disease-modifying Drugs" was accepted in October 2012. In the last 20 months, new targets for the potential treatment of Alzheimer's disease were identified. Enormous progress was realized in the pharmacological characterization of natural products with cognitive enhancing properties. This review covers the evolution of research in this field through May 2014.

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Why calcium channel blockers could be an elite choice in the treatment of Alzheimer’s disease: a comprehensive review of evidences

Cited by 20 publications

References 154 publications

Untitled

Untitled

CX3CL1/CX3CR1 in Alzheimer’s Disease: A Target for Neuroprotection

Cognitive Enhancers (Nootropics). Part 3: Drugs Interacting with Targets other than Receptors or Enzymes. Disease-Modifying Drugs. Update 2014

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